Nutrition and the developing brain: nutrient priorities and measurement  

Oleh:

Georgieff, Michael K.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The American Journal of Clinical Nutrition vol. 85 no. 02 (Feb. 2007), page 614.

Ketersediaan

Perpustakaan FK Nomor Panggil: A07.K.2007.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Nutrients and growth factors regulate brain development during fetal and early postnatal life. The rapidly developing brain is more vulnerable to nutrient insufficiency yet also demonstrates its greatest degree of plasticity. Certain nutrients have greater effects on brain development than do others. These include protein, energy, certain fats, iron, zinc, copper, iodine, selenium, vitamin A, choline, and folate. The effect of any nutrient deficiency or overabundance on brain development will be governed by the principle of timing, dose, and duration. The ability to detect the specific effects of nutrient deficiencies is dependent on knowing which area of the brain is preferentially affected and on having neurologic assessments that tap into the functions of those specific areas. As examples, protein-energy malnutrition causes both global deficits, which are testable by general developmental testing, and area-specific effects on the hippocampus and the cortex. Iron deficiency alters myelination, monoamine neurotransmitter synthesis, and hippocampal energy metabolism in the neonatal period. Assessments of these effects could include tests for speed of processing (myelination), changes in motor and affect (monoamines), and recognition memory (hippocampus). Zinc deficiency alters autonomic nervous system regulation and hippocampal and cerebellar development. Long-chain polyunsaturated fatty acids are important for synaptogenesis, membrane function, and, potentially, myelination. Overall, circuit-specific behavioral and neuroimaging tests are being developed for use in progressively younger infants to more accurately assess the effect of nutrient deficits both while the subject is deficient and after recovery from the deficiency.

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